Stimulation of alpha-2 adrenergic receptors in the brainstem by endogenous catecholamines or antihypertensive drugs causes hypotension and bradycardia as well as a facilitation of the depressor baroreflex response. Opioid peptides on opiates acting in the same brain region have similar effects. Our earlier studies, confirmed by others, indicate that part of the effect of alpha2-adrenergic agonists (e.g. clonidine, alpha-methyldopa) is mediated indirectly through the local release of a beta-endorphin- like opioid. In addition to facilitation of the baroreflex by these two types of substances, there is also evidence for a GABA- mediated inhibition of the baroreflex. Furthermore, there are documented interactions between GABA and the above two neurotransmitters in central cardiovascular control, and all three agents appear to produce their effects at the level of the brainstem. Ethanol has been shown to reduce both beta-endorphin and catecholamine levels in the brainstem, while its neurobehavioral effects have been linked to stimulation of the central GABA- benzodiazepine receptor complex. These observations raise the possibility that the hypertensive effects of ethanol, well establised in population and clinical studies and linked to impaired baroreflex function, may be mediated by its: interaction with central alpha-2, opioid and GABA-ergic mechanisms. We will test this possibility by studying the cardiovascular response to manipulation of these 3 central neurotransmitter systems in control and in chronically ethanol-treated rats.